ArticleNature communications2023
TAZ2 truncation confers overactivation of p300 and cellular vulnerability to HDAC inhibition.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- Structural and functional divergence of cancer hotspot mutations in CREBBP.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- How intrinsically disordered regions shape the function of CREB-binding protein.Biochemical Society transactions · 2026Review
- CBP-IDRs regulate acetylation and gene expression.Cell reports · 2026Article
- Article
- p300: expanding beyond acetylation to mastermind lactylation-dependent tumorigenesis.Frontiers in cell and developmental biology · 2026Review
- Zinc and animal health: an in-depth exploration of its role in physiological functions and regulatory molecular mechanisms.Journal of animal science and biotechnology · 2025Review
- CBP/p300, a promising therapeutic target for prostate cancer.Journal of translational medicine · 2025Review
- KAT6A chimeras form a self-reinforcing epigenetic module with NURF and MLL/COMPASS to sustain AML.Genome biology · 2025Article
- Multiple transactivation domains of EZH2 bind to the TAZ2 domain of p300 and stimulate the acetyltransferase function of p300.The Biochemical journal · 2025Article
- A Novel EP300 Variant in an African American Girl With Global Developmental Delay and Leukemia.Molecular genetics & genomic medicine · 2025Article
- Review
- Targeting lysine acetylation readers and writers.Nature reviews. Drug discovery · 2025Review
- Genetic dysregulation of EP300 in cancers in light of cancer epigenome control - targeting of p300-proficient and -deficient cancers.Molecular therapy. Oncology · 2024Review
- A potent and selective ENL degrader suppresses oncogenic gene expression and leukemia progression.Science advances · 2024Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The histone acetyltransferase p300/CBP is composed of several conserved domains, among which, the TAZ2 domain is known as a protein-protein interaction domain that binds to E1A and various transcription factors. Here we show that TAZ2 has a HAT autoinhibitory function. Truncating p300/CBP at TAZ2 leads to hyperactive HAT and elevated histone H3K27 and H3K18 acetylation in cells. Mechanistically, TAZ2 cooperates with other HAT neighboring domains to maintain the HAT active site in a 'closed' state. Truncating TAZ2 or binding of transcription factors to TAZ2 induces a conformational change that 'opens' the active site for substrate acetylation. Importantly, genetic mutations that lead to p300/CBP TAZ2 truncations are found in human cancers, and cells with TAZ2 truncations are vulnerable to histone deacetylase inhibitors. Our study reveals a function of the TAZ2 domain in HAT autoinhibitory regulation and provides a potential therapeutic strategy for the treatment of cancers harboring p300/CBP TAZ2 truncations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.